Food, family and female age affect reproduction and pup survival of African wild dogs

Understanding factors that affect the reproductive output and growth of a population of endangered carnivores is key to providing information for their effective conservation. Here, we assessed patterns in reproduction for a small population of endangered African wild dogs (Lycaon pictus) over 90 pack years. We tested how availability of prey, pack size, pack density, rainfall, temperature and female age affected the age of first litter, litter size and pup survival. We found that females bred younger when pack density, availability of prey and pack size were large.We also found that fecundity increased significantly with age while the population was male biased only for 1-, 2- and 4-year olds. Larger litters were produced by larger packs, suggesting strong reproductive benefits of grouping related to cooperative hunting and food provisioning for helpers and alpha females. We also found an interaction between breeding female age and pack size where older females in large packs raised a high proportion of pups. Additionally, large litters and large packs were important for raising a greater number of pups to 6 and 12 months, respectively, suggesting that while litter size is important for pup survival, the benefits of a large pack are only realised when pups are older and mobile with the pack. Collectively, these results illustrate the novel finding that prey availability is critically important in initiating reproduction inwild dogs and that the number of non-breeding helpers, female age and litter size is essential to pup survival

Segmental and total uniparental isodisomy (UPiD) as a disease mechanism in autosomal recessive lysosomal

Analyses in our diagnostic DNA laboratory include genes involved in autosomal recessive (AR) lysosomal storage disorders such as glycogenosis type II (Pompe disease) and mucopolysaccharidosis type I (MPSI, Hurler disease). We encountered 4 cases with apparent homozygosity for a disease-causing sequence variant that could be traced to one parent only. In addition, in a young child with cardiomyopathy, in the absence of other symptoms, a diagnosis of Pompe disease was considered. Remarkably, he presented with different enzymatic and genotypic features between leukocytes and skin fibroblasts. All cases were examined with microsatellite markers and SNP genotyping arrays. We identified one case of total uniparental disomy (UPD) of chromosome 17 leading to Pompe disease and three cases of segmental uniparental isodisomy (UPiD) causing Hurler-(4p) or Pompe disease (17q). One Pompe patient with unusual combinations of features was shown to have a mosaic segmental UPiD of chromosome 17q. The chromosome 17 UPD cases amount to 11% of our diagnostic cohort of homozygous Pompe patients (plus one case of pseudoheterozygosity) where segregation analysis was possible. We conclude that inclusion of parental DNA is mandatory for reliable DNA diagnostics. Mild or unusual phenotypes of AR diseases should alert physicians to the possibility of mosaic segmental UPiD. SNP genotyping arrays are used in diagnostic workup of patients with developmental delay. Our results show that even small Regions of Homozygosity that include telomeric areas are worth reporting, regardless of the imprinting status of the chromosome, as they might indicate segmental UPiD

Space Telescope and Optical Reverberation Mapping Project. VII. Understanding the Ultraviolet Anomaly in NGC 5548 with X-Ray Spectroscopy

During the Space Telescope and Optical Reverberation Mapping Project observations of NGC 5548, the continuum and emission-line variability became decorrelated during the second half of the six-month-long observing campaign. Here we present Swift and Chandra X-ray spectra of NGC 5548 obtained as part of the campaign. The Swift spectra show that excess flux (relative to a power-law continuum) in the soft X-ray band appears before the start of the anomalous emission-line behavior, peaks during the period of the anomaly, and then declines. This is a model-independent result suggesting that the soft excess is related to the anomaly. We divide the Swift data into on- and off-anomaly spectra to characterize the soft excess via spectral fitting. The cause of the spectral differences is likely due to a change in the intrinsic spectrum rather than to variable obscuration or partial covering. The Chandra spectra have lower signal-to-noise ratios, but are consistent with the Swift data. Our preferred model of the soft excess is emission from an optically thick, warm Comptonizing corona, the effective optical depth of which increases during the anomaly. This model simultaneously explains all three observations: the UV emission-line flux decrease, the soft-excess increase, and the emission-line anomaly

TRY plant trait database – enhanced coverage and open access

Plant traits—the morphological, anatomical, physiological, biochemical and phenological characteristics of plants—determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait‐based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits—almost complete coverage for ‘plant growth form’. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait–environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

Engineering plants for durable disease resistance

As our knowledge of the cellular and genetic mechanisms of plant disease resistance increase, so does the potential for modifying these processes to achieve broad-spectrum durable disease resistance. A number of approaches have been taken by researchers to identify and understand the complex chain of events that is set in motion when a plant is challenged by a pathogen (Table 18.1) (reviewed by Broekaert et al., 2000; Cornelissen and Schram, 2000; Punja, 2001). Most effort has been applied to studying the constitutive production in transgenic plants of antifungal compounds. These include production of naturally occurring pathogenesisrelated (PR) proteins that may inhibit or prevent pathogen growth in the plant, such as hydrolytic enzymes, antifungal proteins, antimicrobial peptides, ribosome inactivating proteins, and phytoalexins. Others involve the expression of gene products that are either antagonistic to pathogen virulence products, such as polygalacturonase, oxalic acid and lipase, or which enhance the structural defenses within the plant, such as peroxidases and lignins. There has also been research into modifying pathways such as those regulated by salicylic acid, jasmonic acid, ethylene, and hydrogen peroxide that are important in plant defenses. Such resistance mechanisms occur naturally in the plant and the objective is to manipulate the system so that gene products are expressed at levels that defend the plant against pathogen attack, or render the pathogen incapable of attack. Alternative approaches concern the interactions between R genes in plants and the corresponding dominant Avr genes in the pathogen that culminate in the hypersensitive response (HR) in incompatible reactions, and the molecular genotyping of plant lines using DNA-based techniques to facilitate the "pyramiding" of desirable disease resistance traits into elite germplasm